Biomedical Sciences (Physiology)http://hdl.handle.net/10125/869
Wed, 04 Mar 2015 00:06:47 GMT2015-03-04T00:06:47ZUsing RNAi technology to down-regulate Six2 expression in vitrohttp://hdl.handle.net/10125/20439
The Brachyrrhine (Br) mutant mouse, which displays frontonasal dysplasia and renal hypoplasia, has previously been described. Linkage analysis mapped the semi-dominant Br mutation close to the homeobox transcription factor Six2, which is normally expressed in the facial and metanephric mesenchyme during embryonic development. The purpose of this study is to evaluate the role of Six2 in craniofacial and renal branching morphogenesis by quantifying its expression level in the facial prominences and using immunohistochemistry to visualize branching of the ureteric bud in Br mice. In addition, an in vitro system utilizing RNA interference (RNAi) technology was developed to determine whether Six2 could be experimentally down-regulated. Medial nasal (MNP), lateral nasal (LNP) and maxillary prominences (MAX) of EII.5 embryos were dissected and Six2 expression was measured with qRT-PCR. Six2 expression was highest in the MNP, with about 2-fold less in the MAX, and 3-fold less in the LNP of wild-type embryos. Our data indicate a haploinsufficient pattern of Six2 expression in each of the three sets of facial prominences. In addition, kidney organ explants were dissected from E13.5 mouse embryos and immunostained to reveal differences in ureteric bud branching patterns between the three genotypes (+1+, Br/+ and Br/Br). We confirmed a down-regulation of Six2 in a cell culture system utilizing five RNAi constructs. These data indicate a lack of Six2 expression may playa role in the development of a median facial cleft and its reduced effect in the kidney may lead to renal hypoplasia Additionally, an in vitro system was established that will allow experimental down-regulation of Six2 to assess effects on morphogenesis.
Thesis (M.S.)--University of Hawaii at Manoa, 2008.; Includes bibliographical references (leaves 36-42).; vii, 42 leaves, bound 29 cm
Tue, 01 Jan 2008 00:00:00 GMThttp://hdl.handle.net/10125/204392008-01-01T00:00:00ZHynd, Thomas EugeneCompensatory glomerulopathy in 3H1 Brachyrrhine mice with genetic renal hypoplasia is exacerbated by salt treatmenthttp://hdl.handle.net/10125/20438
The Brachyrrhine (Br/+) mice displays a mutation that directly affects the six2 gene, and this results in premature development of the kidneys and nephrons. These mice exhibit renal hypoplasia which is characterized by a reduced kidney volume with a fewer number of nephrons. The purpose of this study is to compare the morphological differences between the 3H1 wild-type (Wt) and Br/+ mice subjected to salt loading. The specific aim of this project is to determine whether salt loading results in glomerulopathy in mice with heritable renal hypoplasia A total of 24 3Hl mice, ranging in age from 12 to 20 weeks, were divided into four groups of 6 mice each: (1) Wt, no salt, (2) Wt, salt-treated, (3) Br/+, no salt and (4) Br/+, salt-treated. The salt-treated groups were given 2% NaCl solution as a sole source of their fluid intake for 5 days while the control animals were given distilled water. After the mice were perfusion-fixed at the end of the 5th day, the kidneys were removed and embedded in paraffin in preparation for histological sectioning. The sections were stained using H&E, and relevant sections were photographed using an Olympus BX41light microscope. The sections were analyzed for the various stereological parameters and analyzed statistically. The fina1 results showed significant differences between the Wt and the Br/+ in kidney volume, glomerular density/number, and glomerular surface area The Wt mice were significantly larger in kidney volume, glomerular density, and glomerular number, while the salt-treated Br/+ were significantly larger in glomerular surface area Results indicate that salt treatment worsens glomerulopathy in the Br/+ mice as a result of compensatory hyperfiltration.
Thesis (M.S.)--University of Hawaii at Manoa, 2008.; Includes bibliographical references (leaves 39-44).; vi, 44 leaves, bound ill. 29 cm
Tue, 01 Jan 2008 00:00:00 GMThttp://hdl.handle.net/10125/204382008-01-01T00:00:00ZKim, Jin SeonDivalent cation channels with intrinsic alpha-kinase activityhttp://hdl.handle.net/10125/12115
Mode of access: World Wide Web.; Thesis (Ph. D.)--University of Hawaii at Manoa, 2005.; Includes bibliographical references (leaves 102-113).; Electronic reproduction.; Also available by subscription via World Wide Web; xvi, 113, pp leaves, bound ill. (some col.) 29 cm
Sat, 01 Jan 2005 00:00:00 GMThttp://hdl.handle.net/10125/121152005-01-01T00:00:00ZBessac, Bret FajansThe role of human serum albumin and its structural variants in coronary heart diseasehttp://hdl.handle.net/10125/12114
Mode of access: World Wide Web.; Thesis (Ph. D.)--University of Hawaii at Manoa, 2004.; Includes bibliographical references (leaves 135-149).; Electronic reproduction.; Also available by subscription via World Wide Web; xvii, 149 leaves, bound ill. 29 cm
Thu, 01 Jan 2004 00:00:00 GMThttp://hdl.handle.net/10125/121142004-01-01T00:00:00ZHa, Ji-SookTemporal effects of prenatal ethanol exposure on the hypothalamo-neurohypophyseal system in the rat (Rattus norvegicus)http://hdl.handle.net/10125/12113
Thesis (Ph. D.)--University of Hawaii at Manoa, 2004.; Includes bibliographical references (leaves 92-105).; Also available by subscription via World Wide Web; xv, 105 leaves, bound ill. 29 cm
Thu, 01 Jan 2004 00:00:00 GMThttp://hdl.handle.net/10125/121132004-01-01T00:00:00ZLim, Jenny MAn analysis of calcium dependent proteolysis in yellowfin tuna (Thunnus albacares) musclehttp://hdl.handle.net/10125/9436
Typescript.; Thesis (Ph. D.)--University of Hawaii at Manoa, 1990.; Includes bibliographical references (leaves 212-221); Microfiche.; xv, 221 leaves, bound ill. 29 cm
Mon, 01 Jan 1990 00:00:00 GMThttp://hdl.handle.net/10125/94361990-01-01T00:00:00ZWatson, Cheryl LynnADH response to peripheral and central cortisol administrationhttp://hdl.handle.net/10125/9435
Cortisol affects water balance, but whether this effect is mediated through antidiuretic hormone (ADH) is unclear. This study examines the response of plasma ADH (pADH) in two groups of conscious dogs; one received cortisol centrally (ivt) in the third ventricle at 300 ng/min, the other peripherally (iv) at 4.16 µg/kg/min, in 4 states of water balance, i.e., dehydration, normal hydration, 5% NaCl iv infusion (0.05 ml/kg/min), and after a water load (40 ml/kg given iv over 30 min), as compared to control experiments without cortisol. Cortisol, either ivt or iv, had no affect on pADH or plasma osmolality (pOsm) during dehydration or normal hydration. Ivt cortisol infusion caused a progressive decline in plasma cortisol (pCort) while iv cortisol infusion increased pCort (control 2.0 µg%, ivt pCort 0.5 µg%, iv pCort 17 µg%, P<0.01). During the 5% NaCl iv infusion, pADH and pOsm increased similarly in both the control and ivt cortisol experiments from 1.0 to 1.9 µU/ml and 295 to 305 mOsm/kg H2O, respectively (P<0.01). The increase in pADH seen with 5% NaCl infusion was delayed in the iv cortisol experiment as compared to the iv control (75 min versus 45 min, P<0.01). This delay was also seen in pOsm; 45 min in iv cortisol versus 15 min in iv control (P<0.01), indicating that the elevated pCort apparently delays the development of increased pOsm and the subsequent increase in pADH. During a water load, the cumulative urine excreted was 99% of that ingested with iv cortisol (P<0.05), 82% in the control, and 70% with ivt cortisol; in all three cases similar decreases in pADH and pOsm occurred. The free water clearance (FWC) was augmented in the iv cortisol infusion and attenuated in the opposite situation of pCort insufficiency which was established during the ivt cortisol infusion. Thus, the present study demonstrates that cortisol has a peripheral effect in that elevated plasma cortisol 1) delays the rise in pOsm during hypertonic saline infusion 2) increases FWC during a water diuresis but 3) does not alter the pADH versus pOsm relationship, therefore 4) affects the ability to excrete a water load independent of ADH. These data are compatible with a mechanism in which excess cortisol enhances the Na+ "leak" pathway of the cells by increasing the membrane permeability to Na+, thereby increasing the osmolar content of the cells.
Typescript.; Bibliography: leaves 135-147.; Photocopy.; Microfilm.; xiv, 147 leaves, bound ill. 29 cm
Thu, 01 Jan 1987 00:00:00 GMThttp://hdl.handle.net/10125/94351987-01-01T00:00:00ZCornette-Finn, Kuuleialoha MThe role of complement and neutrophils in air bubble-induced lung injuryhttp://hdl.handle.net/10125/9433
Pulmonary air embolism causes vascular obstruction and induces biochemical reactions leading to lung injury. In the present study, by using isolated and perfused rat lungs, we investigated the involvement of the complement system and polymorphonuclear leukocytes (P:MN) in the alterations of segmental vascular resistances, lung weight gain, and filtration coefficient (K), a measure of vascular permeability. After establishing ventilation with air and 5% CO2, the lung was removed en bloc and suspended in a humidified chamber at 37°C. Lung weight, arterial and venous pressures were monitored continuously. Lungs were perfused with physiological salt solution (PSS) containing 4% Ficoll. We used 6 series of perfusates containing: 1) PSS, 2) PMN, 3) plasma, 4) decomplemented plasma, 5) PMN and plasma, and 6) PMN and decomplemented plasma. Air embolism, induced by a 0.76-ml air infusion to arterial catheter in 20 min, increased arterial pressure without altering capillary and venous pressure, suggesting that the increased arterial resistance alone was responsible for the pulmonary hypertension. In lungs perfused with both PMN and normal plasma, air embolism increased Kf by 145 ± 190% which was significantly greater than those in lungs perfused with either PMN (91 ± 8%), plasma (90 ± 8%), or PMN and decomplemented plasma (80 ± 9%). Air embolism increased Kf by 45 ± 12% in the lungs perfused with decomplemented plasma, which was the least among groups. These results suggest that air embolism damages the lung by hypertension, activation of the complement, and activation of PMN, singly or in combinations. The modulation role of PMN in air bubble-induced lung injury was investigated by pretreating the lungs with blocking agents of the cytotoxic substances released from PMN. The lungs perfused with both P:MN and normal plasma served as the control group. In lungs pretreated with scavengers, air embolism increased Kr by 108 ± 25% which was not different from the control group. Air embolism induced little change of Kf in the lungs pretreated with indomethacin (17 ± 8%) or isoproterenol (0 ± 9%), suggesting that air embolism increases pulmonary vascular permeability involving the release of arachidonic acid metabolites.
Thesis (Ph. D.)--University of Hawaii at Manoa, 1995.; Includes bibliographical references (leaves 149-171).; Microfiche.; xvi, 171 leaves, bound ill. 29 cm
Sun, 01 Jan 1995 00:00:00 GMThttp://hdl.handle.net/10125/94331995-01-01T00:00:00ZHuang, Kun-LunBioenergietics of the bottlenose dolphin (Tursiops truncatus)http://hdl.handle.net/10125/9432
There are numerous species of marine mammals found throughout the earth's oceans and waterways. The study of marine mammal energetics is an attempt to define the flow of energy in homeotherms adapted to an aqueous environment. Their lifestyle is different than terrestrial mammals and must compensate for the challenging thermoregulatory requirements of water survival. Field studies of free-ranging animals are difficult, since continual direct observation and measurements are impossible. It is important to conduct controlled laboratory studies, from which to build a foundation of physiological principles on these mammals. The objectives of this research project were to investigate the bioenergetic scheme of the bottlenose dolphin under controlled laboratory-like conditions. Morphometric data in a large bottlenose dolphin population established an equation to predict age from length measurements in juvenile animals. The decrease in caloric intake seen with aging is in agreement with terrestrial mammals, and the importance of nutritional planning based on calories per kilogram body weight versus total calories fed was explained. Increased activity levels required increased caloric consumption, the amount being related to the degree of activity. A recently developed method to assess blubber volume using ultrasound are compared to standard measurements of body condition, weight-length ratio and condition index, and found to be a valid technique in this species. Blubber insulation was found to be more important than surface area in controlling environmental heat loss. Using stable isotopes of water, body composition, lean body mass and fat mass, were determined. An increase in fat mass, with a concurrent decrease in lean body mass, was observed in adult bottlenose dolphins, similar to terrestrial mammals. Also, consumption of a high fat diet contributed to an increase in body fat. Metabolic rates declined with age in bottlenose dolphins, and a significant increase was observed with low fat diets. Finally, the use of doubly labeled water to determine metabolic rate in free-ranging bottlenose dolphins was compared to the intake balance method and found to be an accurate technique in this species. The drawbacks of controlled laboratory trials is that, although all attempts are made to mimic diets and conditions that exist in the wild, the methods are only an approximation of wild conditions. The advantages are the ability to isolate and evaluate individual parameters and ensure adequate and timely data collection. It is essential to combine laboratory and field studies in order to elucidate the bioenergetic mechanisms and physiological adaptations of marine mammals. Although marine mammals have evolved specialized compensatory adaptations to ensure success in an aquatic environment, they follow the same general principles observed in terrestrial mammals. This research supports the concept of evolution and the relationship of all homeotherms, despite differences in ecological niches.
Title printed with error on title page: "Bioenergietics of the bottlenose dolphin (Tursiops truncatus)"; Thesis (Ph. D.)--University of Hawaii at Manoa, 1995.; Includes bibliographical references (leaves 131-143).; Microfiche.; xii, 143 leaves, bound 29 cm
Sun, 01 Jan 1995 00:00:00 GMThttp://hdl.handle.net/10125/94321995-01-01T00:00:00ZMagee, Michelle CoyneCardiorespiratory responses to slight expiratory resistive loading during strenuous exercise at sea levelhttp://hdl.handle.net/10125/9431
At sea level we determined the cardiorespiratory and performance effects of a slight expiratory resistive load (ERL) which, at mild altitude, had been effective in mitigating exercise-induced hypoxemia (EIH). Paired VO2max bicycle ergometer tests, (ERL vs control) were performed by 28 highly-fit (VO2max = 63.4 ±. 1.36) athletes (age = 33.5 ± 7.3). There was significant EIH in both control and ERL tests at 75, 80, 85. and 90% maximum power output (POmax) and at VO2max when compared to resting SaO2; but no difference in SaO2 between control and ERL at any level of intensity. Peak-expiratory mouth pressures (Pao) were greater (p≤0.05) with ERL at 75, 80, 85, 90 % POmax and VO2max: with ERL, Pao was increased compared to control by 0.20, 0.35, 0.41, 0.49, and 0.73 cm H2O, respectively. Concomitantly, minute ventilation (VE) was greater with ERL vs control (p≤0.05) by 4.1, 4.9, 4.5, and 5.8 L min^-1 at 80, 85, 90 % POmax and VO2max. The increase in VE was largely due to a trend toward increased tidal volume (.1 ml = 121, 198, 154, and 103, from 75 to 90 % POmax). There was a small, non-significant increase in VO2 (averaging 3.0 ml kg^-1-sec^-1) with ERL from 75-90 % POmax. With ERL, heart rate (HR) was consistently lower (≥ 2.0 BPM) throughout, although not significantly so. However, O2 pulse (VO2/ HR) was significantly greater with ERL by 9.5, 9.0, 7.9, 7.1 and 7.0 % at 75, 80, 85, 90 % POmax and V02max. With ERL, athletes attained greater (p ≤ 0.05) POmax 352.0 ±. 9.9 vs 345.7 ±. 9.5 watts, and higher (p ≤ 0.05) VO2max = 63.4 ±. 1.36 vs 60.3 ±. 1.26 ml kg^-l min^-1. Subsequently, in a subset (n =12), FRC was determined by He-dilution during steady-state 75 % POmax. With ERL, Pao VE, and VT/Te were greater (p<0.05) and FRC was elevated (p≤0.05) 0.67 ±. 0.29 L. End-inspiratory lung volume (EILV) with ERL was greater than control (p≤0.05), 82.2 ±. 1.1 vs 72.5 ±. 1.3 % of TLC, respectively. We conclude that during heavy to intense exercise, surprisingly small ERL (ranging from 1.27 to 2.94 cm H2O) may cause VT to increase and FRG to shift upward, reducing the potential for air flow limitation. That O2 pulse was higher with ERL at workloads identical to that of control, would suggest that venous return was augmented, perhaps in response to reduced pulmonary vascular resistance associated with increased FRG. The significantly improved VO2max with ERL may be due in part to the increased inspiratory work of breathing that exercising at elevated FRCs may entail; however, it would appear that some fraction of the increased VO2max observed with ERL was delivered to the working skeletal muscle which produced significantly greater POmax. We conclude that during strenuous exercise, slight expiratory resistive loading enhances performance in highly-trained athletes.
Thesis (Ph. D.)--University of Hawaii at Manoa, 1995.; Includes bibliographical references (leaves 96-106).; Microfiche.; xxii, 106 leaves, bound 29 cm
Sun, 01 Jan 1995 00:00:00 GMThttp://hdl.handle.net/10125/94311995-01-01T00:00:00ZFee, Larry LThe effect of age and gender on the peripheral blood cell response to Escherichia Coli lipopolysaccharide (LPS) in Wistar rats (Rattus Norvegicus)http://hdl.handle.net/10125/9430
Escherichia coli (E. coli) lipopolysaccharide (LPS) is the major component of mammalian gut bacterial flora. Inflammatory diseases of unknown etiology, e.g., rheumatoid arthritis, may be triggered by periodic transmural release of LPS from the gut into the peritoneal cavity. If so, an older animal should have a greater exposure history to LPS and, therefore, be hyper-responsive. Age and gender-related variation in peripheral blood cell responsiveness was determined in untreated rats (time zero). The acute (0-2 day) and long-term (3-24 day) response to an intraperitoneal injection of 0.5 mg/kg E. coli LPS was compared to control (sterile 0.9% saline) in young, middle-aged, and old male and female Wistar rats. In untreated rats, a number of parameters changed with age: older rats had increased white blood cell (WBC) chemiluminescence (CL) , time-to-peak CL, plasma protein concentration, and decreased WBC total count, and in vitro WBC mobility. Packed cell volume (PVC) increased in middle-age, but decreased in old rats. Saline-treated male rats had higher WBC counts, body weight, CL, and PVC when compared to age-matched, saline-treated, female rats. Acutely, LPS caused a hypothermia in all rats, which was more profound and prolonged in the old rats. Hypothermia was followed by fever, which was highest in the young rats. LPS also increased WBC counts and CL, and decreased time-to-peak WBC CL in all rats. WBC CL was greater in old and middle-aged rats during days 13-24 following LPS. Blood-free, homogenized, liver cell CL tripled in old age. These findings suggest that LPS was a pro-inflammatory stimulant, particularly in the middle-aged and old rats. Interestingly, this effect of LPS appears to eliminate many age and gender effects noted in the untreated animals. The observation that a single I.P. injection of LPS has no effect on WBC CL during the first three hours and increases CL during hours 3-48 in all but the old female group, and that the old female rats' WBC CL was depressed during the first 12 hours and enhanced at hour 48, may explain some of the conflicting observations made by others using shorter protocols.
Thesis (Ph. D.)--University of Hawaii at Manoa, 1994.; Includes bibliographical references (leaves 147-160).; Microfiche.; xvii, 160 leaves, bound ill. 29 cm
Sat, 01 Jan 1994 00:00:00 GMThttp://hdl.handle.net/10125/94301994-01-01T00:00:00ZMerritt, Deborah JComparative physiology of dipeptide transport in lower vertebrates (fishes) and invertebrates (lobster)http://hdl.handle.net/10125/9429
In my study I propose to undertake an investigation to characterize the brush border uptake and basolateral efflux mechanisms of a biologically stable dipeptide, glycylsarcosine in an herbivorous teleost (tilapia, Oreochromis mossambicus.). This will be the first study to characterize dieptide uptake and efflux processes of a single dipeptide in any animal. In order to extend our understanding of such a unique system, I would like to compare the characteristics of brush border uptake in the herbivorous tilapia to those of a carnivorous teleost (rock fish, Sebastes caurinus) and an omnivorous invertebrate (lobster, Homarus americanus). The lobster hepatopancreas is a diverticulum of the pyloric stomach. Over the past few years a number of studies have focused on the mechanism of sugar and amino acid transport by hepatopancreatic BBMV (4,5). These investigations showed that the hepatopancreas plays a major role in the absorption of nutrients in this animal. A novel feature of these diverticula is that the luminal pH at times of feeding may drop to as low as 4 (18). A number of studies have shown that a drop in external pH stimulates sugar and amino acid transport into hepatopancreatic BBMV. The observed stimulation was attributed either to protonation of amino acids with the protonated form being the preferred substrate, or protonation of the carrier resulting in an increase in the binding affinity for the sugars. The acidic nature of these diverticula at the absorptive site, markedly affecting nutrient transport, make this an ideal animal model since the solutes under investigation (dipeptides) are known to be coupled to protons in other types of animals. It will be of interest to investigate: (1) whether such a proton coupled dipeptide mechanism exists in the brush border membrane of lobster hepatopancreas, (2) If so, are the affinities and transport capacities of these dipeptide transporters any different than those described for mammals and fishes, (3) Does the binding affinity of this transporter show any variation at different pH values?, and (4) Is the specificity of this transporter any different from those exhibited by vertebrates?
Thesis (Ph.D.)--University of Hawaii at Manoa, 1994.; Includes bibliographical references (leaves 112-114).; Microfiche.; xi, 117 leaves, bound ill. 29 cm
Sat, 01 Jan 1994 00:00:00 GMThttp://hdl.handle.net/10125/94291994-01-01T00:00:00ZThamotharan, ManikkavasagarAlcohol metabolism in a multi-ethnic population : simultaneous determination of plasma ethanol, acetaldehyde and acetate using gas chromatography in subjects of Asian and European descent and correlation of concurrent cardiovascular responseshttp://hdl.handle.net/10125/9428
Thesis (Ph. D.)--University of Hawaii at Manoa, 1994.; Includes bibliographical references (l. 241-251); Microfiche.; 251 leaves, bound illus. 29 cm
Sat, 01 Jan 1994 00:00:00 GMThttp://hdl.handle.net/10125/94281994-01-01T00:00:00ZFairman, Colin LCardiovascular and hormonal responses to hypotension during hypoxia in the conscious goathttp://hdl.handle.net/10125/9427
The cardiovascular and hormonal responses to hemorrhage and chemically-induced hypotension in conscious goats were assessed in the present study. A progressive hemorrhage (0.5 ml/kg/min for 30 min) under hypoxic (FiO2=0.10) conditions (HH, n =4) reduced mean arterial blood pressure (MABP) after only 20 min of blood loss. An identical hemorrhage under normoxic conditions (NH, n =4) did not reduce MABP until after the blood loss was complete. Heart rate (HR) was significantly increased with hemorrhage only during normoxia. Arginine vasopressin (AVP) responses followed MABP chances, with HH levels being greater at an earlier time point. Final AVP values were not different between NH and HH. Plasma renin activity (PRA) responded in near identical fashion between the two settings, despite the earlier reduction in MABP with HH. Atrial natriuretic factor (ANF) was reduced during hemorrhage with both exposures. Sodium nitroprusside (SNP) infusions sufficient in reducing MABP 20% increased HR only during normoxia (NH, n =4). HR was not changed with hypotension during hypoxia (HH, n =4). AVP levels were increased with SNP infusions during both exposures, with HH values greater than NH. PRA and epinephrine (EPI) increased in similar fashion during NH and HH. Norepinephrine (NE) and ANF were unchanged with SNP induced hypotension. Finally, an acute 60 minute hypoxic exposure increased HR within the first 10 minutes. No transient increases in MASP, plasma NE or EPI were detected over the 60 min period of hypoxia. Thus, hemorrhage during hypoxia poses a greater challenge to the cardiovascular system than does an equal blood loss during normoxia. Further, it appears that hypoxia attenuates the PRA response to hemorrhage. However, when MASP is reduced over an identical time frame during normoxia and hypoxia, no differences in the PRA responses can be observed, while a hypoxic augmentation of the AVP response to hypotension becomes apparent. Finally, the data suggest a hypoxic attenuation of the arterial baroreflex tachycardia with hypotension in conscious goats.
Thesis (Ph. D.)--University of Hawaii at Manoa, 1993.; Includes bibliographical references (leaves 147-159); Microfiche.; xii, 159 leaves, bound ill. 29 cm
Fri, 01 Jan 1993 00:00:00 GMThttp://hdl.handle.net/10125/94271993-01-01T00:00:00ZEichinger, Mark RRelaxin and prolactin secretion from the human decidual cell : regulation in vitrohttp://hdl.handle.net/10125/9426
A cell immunoblot technique originally designed for the study of prolactin secretion by rat pituitary cells has been modified and evaluated for the study of relaxin and prolactin accumulation and secretion from individual human decidual cells in vitro. Prolactin has been studied extensively in the human decidua, however nothing is known about the regulation of relaxin secretion. Macrophages were shown to make up 25% and chorionic cytotrophoblasts 10% of the cells in the decidual cell preparation. The decidual cells analyzed were selected by size and absence of immunostaining with macrophage and cytotrophoblast cell markers. Relaxin and prolactin intracellular accumulation and secretion were detected immunocytochemically as intracellular and extracellular staining respectively and were quantitated with an IBAS Kontron image analysis system. Relaxin secretion was detected after 15 min of incubation and was unaffected by cycloheximide suggesting release of preformed hormone. Prolactin on the other hand was only detected intracellularly up to 18 h and this was decreased by cycloheximide suggesting new production synthesis. Relaxin intracellular accumulation and secretion were significantly increased when the cells were incubated with added porcine relaxin, H2 synthetic human relaxin and Hl recombinant human relaxin. Porcine relaxin was slightly more potent than human H2 relaxin, which was more potent than the Hl synthetic peptide in increasing its own synthesis and secretion in vitro. Human and porcine insulins also significantly increased relaxin intracellular and extracellular staining. Preliminary results of added IGF-l and EGF showed stimulatory effects on relaxin intracellular and extracellular staining, but these results were not dose-dependent and are therefore questionable. Exogenous prolactin had both stimulatory and inhibitory effects on relaxin accumulation and secretion, and caused a significant increase in prolactin accumulation without affecting its secretion. The results suggest that relaxin and prolactin may be autocrine hormones in the human decidua, and the effects of relaxin treatment provide indirect evidence for the presence of relaxin receptors on the decidual cells. Preliminary results of treatment with insulin, IGF-l and EGF also suggest that these hormones may act as paracrine regulators of decidual relaxin synthesis and secretion.
Thesis (Ph. D.)--University of Hawaii at Manoa, 1992.; Includes bibliographical references.; Microfiche.; xiii, 191 leaves, bound ill. 29 cm
Wed, 01 Jan 1992 00:00:00 GMThttp://hdl.handle.net/10125/94261992-01-01T00:00:00ZHijazi, Mai MResponses of water and salt regulating hormones during acute cold exposure in the rathttp://hdl.handle.net/10125/9425
Soon after exposure to cold, humans and some animals experience a dilute diuresis, which is often accompanied by a natriuresis. Plasma vasopressin has been reported to decrease, possibly due to a central shunting of blood from peripheral vasoconstriction, and subsequent activation of the "Gauer-Henry reflex". The sodium regulating hormones atrial natriuretic factor (ANF), and the renin-aldosterone system have not been measured acutely in the cold. The present study used the conscious, chronically instrumented rat to assess plasma vasopressin, aldosterone, renin, ANF, and urinary vasopressin during acute cold exposures of 1 hour at 13° C., or time control at 26° C.. Urine flow, osmolality, electrolyte excretion rates, and creatinine, osmotic, and free water clearances were measured at 10 minute intervals. Hematocrit, plasma electrolytes and osmolality, and all hormones were obtained using a donor replacement protocol at baseline, at 20, and 60 minutes of cold exposure, and at 1 hour recovery. Rectal temperature, heart rate, and mean arterial blood pressure were monitored, and to evaluate the degree of cold-induced thoracic engorgement, central venous pressure was measured in one series of experiments. In all series of experiments, urine flow increased to double or more baseline values by 20 minutes of cold exposure (p < .05). By 60 minutes, in the cold, however, flow had returned toward baseline, and was different neither from baseline nor from time control. The free water component of the diuresis followed the same pattern, while urinary osmolality decreased biphasically as well. Osmotic clearance significantly increased in all series, and creatinine clearance was unchanged. Plasma vasopressin was significantly reduced compared to baseline at 20 minutes of cold exposure in all three series in which it was measured. Values had returned to baseline levels by 60 minutes in the cold. Mean arterial blood pressure and heart rate increased significantly in the cold (p < .01), while all but one experimental series showed no change in plasma osmolality, and in no series was there a change in rectal temperature. Mean central venous pressure was unaffected by cold exposure, although systolic and pulsatile central venous pressure increased. Cold was without effect on sodium excretion, with both control and cold-exposed groups significantly increasing their rate of excretion. Similarly, there was no change in plasma ANF, although both renin and aldosterone increased progressively during cold exposure. These results suggest that there is no consistent natriuresis in the rat during acute cold exposure, and that an increase in arterial blood pressure may be the driving force behind the observed reductions in plasma vasopressin.
Thesis (Ph. D.)--University of Hawaii at Manoa, 1992.; Includes bibliographical references (leaves 133-145); Microfiche.; xvi, 145 leaves, bound ill. 29 cm
Wed, 01 Jan 1992 00:00:00 GMThttp://hdl.handle.net/10125/94251992-01-01T00:00:00ZDice, Margaret SEffects of electromagnetic fields and temperature on avian embryonic growth and oxygen consumptionhttp://hdl.handle.net/10125/9424
Domestic fowl embryonic growth, oxygen consumption, body dimensions and organ (including pectoral and leg muscles) dry/wet mass, heart rate, respiratory rate and growth abnormalities were studied at altered incubation temperatures (36 °C,40 °C) and after exposure to 2.0, 1.0 and 0.5 gauss (G) electromagnetic fields (EMF), from the seventh day of incubation to hatching. Embryonic organ growth was promoted when incubation temperature was increased from 38°C (control) to 40 °C, but organ growth was significantly retarded when incubation temperature was decreased from 38°C to 36 °C. Evidence was obtained that some tissues (eyeballs and heart) were "spared" the reduction in growth at 36°C, while the lungs, eyeballs and pectoral muscles were spared the accelerated growth at 40 °C. The maturity of the organs (as assessed by their dry/wet mass ratios) was, like their growth, less at 36°C than at 38 °c and this was particularly evident in leg muscle and liver. Organ maturity was enhanced at 40°C especially in the pectoral muscles and stomach. The hatchability of eggs incubated at 36°C was impaired. Embryonic growth and oxygen consumption were increased after exposure to a 2.0 G EMF but inhibited in the 1.0 G EMF group. There were no significant biological effects of 0.5 G EMF on embryonic growth and oxygen consumption. Deformities were found in the 2.0 G and 1.0 G EMF groups but only in the 2.0 G group did reach a statistically significant level. There were no deformities in the 0.5 G EMF group or any of the control groups. The heart and lungs were spared the enhanced overall growth induced by exposure to a 2 G EMF while the intestine was spared the repression of growth at an EMF of I G. Enhanced organ growth was associated with increased tissue maturity, particularly in pectoral muscle and the intestine. The effects of a 1 G EMF on organ maturity were small but, paradoxically, lung maturity increased. A number of deformities was noted in embryos exposed to 2 G EMF. Incubation at 40°C and exposure to a 2 G EMF both increased embryonic growth while incubation at 36°C and exposure to 1 G EMF both repressed growth, overall. However, there were few similarities in the specific effects of the two growth-promoting/ repressing agents on organ growth and maturity. A major difference between temperature ,and EMF was that they exerted their effects at different stages of embryonic life. No significant effects of either temperature or EMF were observed on heart rates, respiratory rates or tissue histology.
Thesis (Ph. D.)--University of Hawaii at Manoa, 1992.; Includes bibliographical references (leaves 202-210); Microfiche.; xvii, 210 leaves, bound ill. (some col.) 29 cm
Wed, 01 Jan 1992 00:00:00 GMThttp://hdl.handle.net/10125/94241992-01-01T00:00:00ZZhang, QinggenChanges in hormone excretion in swimmers over the course of a training seasonhttp://hdl.handle.net/10125/9423
The purpose of this study is to investigate the change in catecholamine levels over the course of a training season in collegiate swimmers. Swimmers were chosen because there are no reports in the literature that look at the response to stress in actively training swimmers. Additionally, there are very few studies which use athletes trained at the intensity of collegiate swimmers (27, 64, 156). Thus, one of the first requirements of the study was to obtain data on collegiate swimmers training at elite levels. The study was designed to determine the long term changes in hormone secretion patterns when the intensity of training was continually increased. There are no reports of studies on athletes training for more than four months duration (287). Since most elite athletes train for much longer periods of time than four months, the first objective was to develop a research protocol that would result in information on catecholamine production over an extended period of time. A second objective was to test for a relationship between a simple psychological measure and the results obtained from physiological measurements. Since there are no reports about the psychological changes in elite athletes during a training season, a third objective was to determine if there was any correlation between psychological and physiological changes. A fourth objective was to evaluate whether a testing day could be broken into time periods and then assess if there was a particular time period of the day when there was more or less change due to stress. Although a few reports have described the variation in secretion in sedentary subjects with time of day (86, 104,183), none have looked at this variation in elite athletes. A fifth objective was to determine what variable or variables correlated with hormone secretion. Was it distance trained, psychological stress, time of day, or some other factor? Again, no one has reported attempting to determine the relationship of catecholamines to other variables in elite athletes. The last objective of this study was to determine whether any observed changes in catecholamine output were due to changes in production or to changes in metabolism. By measuring the metabolites of norepinephrine and epinephrine, it was anticipated that the factors responsible for changes in hormone excretion could be determined. Thus. this research sought to test three main hypotheses. First: there is a change in catecholamine production in swimmers throughout the training season. Second: this change could be correlated to changes in psychological stress evaluations and to the amount of distance trained. Finally: the change in catecholamine production could be directly correlated to a change in catecholamine metabolite production.
Thesis (Ph. D.)--University of Hawaii at Manoa, 1991.; Includes bibliographical references (leaves 142-163); Microfiche.; xi, 163 leaves, bound ill. 29 cm
Tue, 01 Jan 1991 00:00:00 GMThttp://hdl.handle.net/10125/94231991-01-01T00:00:00ZHale, DavidSodium channel activation mechanisms : insights from deuterium oxide and delta-9-tetrahydrocannabinol substitutionhttp://hdl.handle.net/10125/9422
Schauf and Bullock (1979, 1982) demonstrated that solvent substitution with deuterium oxide (D2O) significantly affects both sodium channel activation and inactivation kinetics without corresponding changes in gating current or tail current rates. They concluded, (a) no significant component of gating current derives from the final channel opening step and, (b) channels must deactivate (during tail currents) by a different pathway from that used in channel opening. By contrast, Oxford (1981) found in squid axons that, when a depolarizing pulse is interrupted by a brief return to holding potential, subsequent reactivation is very rapid and shows almost monoexponential kinetics. Increasing the interpulse interval resulted in secondary activation rate returning towards control, sigmoid kinetics. He concluded that channels open and close via the same pathway. I have repeated both sets of observations, confirming the results obtained in both previous studies, despite the apparently contradictory conclusions reached by these authors. However, I find that secondary activation following a brief interpulse interval is insensitive to D20, although reactivation following longer interpulse intervals returns towards a D20-sensitivity similar to that of primary activation. I conclude that D20sensitive primary activation and D20-insensitive tail current deactivation involve separate pathways. However, D20-insensitive secondary activation involves reversal of the D20-insensitive deactivation step. Strichartz et al. (1978) were the first to investigate the effects of delta-9tetrahydrocannabinol (THC) on sodium channel conductance mechanisms under voltage-clamp conditions. The authors reported that THC modified channel conductance by slowing the activation kinetics of INa and suppressing ionic conductance (gNa) in a voltage-dependent manner. They also noted that channel inactivation processes were not affected by THC action. The authors concluded that the lengthening of !p and the shift in the voltage-dependence of peak gNa are both related to the relative kinetics of sodium activation and inactivation, and since inactivation was unaffected by THC, alterations of activation alone account for these observed changes. I have repeated the above observations, but I can confirm only one of the three results obtained in the previous studies. I find that THC affects both activation and inactivation kinetics. However, I find that the normalized F(Vm) curves are almost identical indicating no significant shift in surface charge following THC treatment.
Thesis (Ph. D.)--University of Hawaii at Manoa, 1990.; Includes bibliographical references (leaves 135-153); Microfiche.; xi, 153 leaves, bound ill. 29 cm
Mon, 01 Jan 1990 00:00:00 GMThttp://hdl.handle.net/10125/94221990-01-01T00:00:00ZAlicata, Daniel AndrewBioenergetics of the Hawaiian monk seal (Monachus schauinslandi)http://hdl.handle.net/10125/9421
Thesis (Ph. D.)--University of Hawaii at Manoa, 1990.; Includes bibliographical references.; v. 1. Energetics and adaptation -- v. 2. The average daily metabolic rate and associated energy substrate utilization as determined by the doubly labeled water technique.; Microfiche.; 2 v. bound ill. (some col.) 29 cm
Mon, 01 Jan 1990 00:00:00 GMThttp://hdl.handle.net/10125/94211990-01-01T00:00:00ZDunn, Ronald ECardiovascular and respiratory responses to hypoxia in three species of obligate ram ventilating fishes, skipjack tuna (Katsuwonus pelamis), yellowfin tuna (Thunnus albacares), and bigeye tuna (T. obesus)http://hdl.handle.net/10125/9420
Typescript.; Thesis (Ph. D.)--University of Hawaii at Manoa, 1988.; Includes bibliographical references.; Microfiche.; xvii, 276 leaves, bound ill. (some ill.) 29 cm
Fri, 01 Jan 1988 00:00:00 GMThttp://hdl.handle.net/10125/94201988-01-01T00:00:00ZBushnell, Peter GeraldThe metabolic clearance of arginine vasopressin in the amniotic sac of the fetal guinea pighttp://hdl.handle.net/10125/9419
A route for arginine vasopressin (AVP) clearance in the fetus has yet to be established. Ervin et ale (Am. J. Physiol. 250:E253-8, 1986) reported that AVP may be absorbed in the ovine fetal gut and remain biologically active. Thus, an AVP clearance problem could exist in the fetus since fetal urinary AVP may be recirculated. The results of the present study indicate that in the fetal guinea pig AVP is metabolized in the amniotic sac. When fetal urine and amniotic fluid (AF) were fractionated on HPLC, AVP was identified only in fetal urine. Moreover, when AVP and inulin were injected into the AF in vivo during the last week of gestation, the AVP/inulin ratio decreased (regression, p=0.01) over a 2 hour period, indicating a swallowing-independent disappearance of AVP. Also, the rate of AVP disappearance increased (regression, p<0.01) with increasing initial AF AVP concentration. When tritiated AVP was similarly injected, the radioactivity/inulin ratio remained constant, suggesting that AVP was not diffusing out of the amniotic sac. Two hours after the injection the AF was collected and fractionated by HPLC, and only 42% of the total radioactivity was intact AVP. The remainder was identified in 2 other products (M1 and M2). Tritiated AVP incubated with AF and amnionic membrane in vitro produced both Ml and M2. Tritiated AVP incubated with amnionic membrane in artificial amniotic solution produced Ml with no M2. Tritiated AVP incubated in only AF produced M2 with no MI. Thus, neither metabolite was necessary for the production of the other, Ml was amnionic membrane dependent and M2 was AF dependent. The amnionic membrane metabolic system was functioning as early as 34 days of gestation (term = 68 days) whereas the AF enzyme system was not effective until 54 days of gestation, further support that the 2 metabolic systems are independent of each other. M2 comigrates with des-glycinamide AVP in three different HPLC buffers and crossreacts only with an AVP antiserum that detects des-glycinamide AVP. M2 production in the amniotic fluid can be blocked with the trypsin inhibitor aprotinin, suggesting that the amniotic fluid enzyme responsible for M2 production is trypsin-like. In establishing the guinea pig as an animal model, amniotic fluid osmolality (OSM), and sodium (Na), potassium (K) and cortisol concentrations were measured in the second and third trimesters of gestation. Amniotic fluid OSM did not change and K concentration increased (regression, p<0.01) with gestational age in contrast to reported human values in which OSM decreased and K remained constant with age. Amniotic fluid Na levels decreased (regression, p<0.01) and cortisol levels increased (regression, p<0.01) with age in the guinea pig, similar to results reported in humans. Fetal plasma and urine OSM, Na and K were also measured in the late third trimester. Fetal urine was found to be slightly hypertonic compared to fetal plasma (328 ± 8 m0sm/kg H2O vs. 308 ± 3 mOsm/kg H2O, p<0.05), and urinary Na concentration was lower than fetal plasma (127.2 ± 1.0 mEq/l vs. 139.9 ± 0.4 mEq/l, p<0.05), which indicated that the guinea pig fetal kidney or bladder may be involved with the reabsorption of water and Na. Some other undetermined osmotically active substances besides Na and K are responsible for most of the fetal urine osmotic activity since Na, K, and attendant anions account for less than 15% of the urine osmolality. A difference was discovered between Na and K levels in the amniotic fluid and fetal urine: although fetal urine was hypertonic to amniotic fluid (328 ± 8 mOsm/kg H2O vs. 287 + 2 mOsm/kg H2O, p<0.05), urinary Na and K concentrations were lower than amniotic fluid concentrations (by 115.8 mEq/l and 6.3 mEq/l, respectively). Therefore, fetal urine is modified in the amniotic sac. Amniotic fluid OSM measured in fetuses in the late third trimester was constant (287±2 mOsm/kg H2O) despite a large variation in urine osmolalities (288 to 393 mOsm/kg H2O). The regulation of amniotic fluid OSM is not well understood but a hormonal regulation of water and electrolyte movement across the amnion is believed to be involved. The present study was unable to demonstrate an influence of amniotic fluid AVP on amniotic fluid OSM. In conclusion, the amniotic sac may play a role in the clearance of AVP, as well as the clearance of other proteins, from the fetal system. Amniotic fluid OSM appears to be tightly regulated and the mechanisms behind this regulation remain unresolved.
Typescript.; Bibliography: leaves 158-169.; Photocopy.; Microfilm.; xviii, 169 leaves, bound ill. 29 cm
Thu, 01 Jan 1987 00:00:00 GMThttp://hdl.handle.net/10125/94191987-01-01T00:00:00ZUyehara, Catherine F. TLung-derived growth factors : possible paracrine effectors of fetal lung developmenthttp://hdl.handle.net/10125/9418
Morphogenesis involves the specific arrangement of embryonic cell populations which ultimately results in organs with unique structures. Substantial evidence suggests that cell and tissue interactions are the primary regulatory mechanisms for the developmental process. A potential role for paracrine secretions in lung organogenesis has been hypothesized (Alescio & Piperno, 1957). These studies present direct support for the paracrine model by demonstrating the presence of locally produced mitogenic/maturational factors in fetal rat lung tissue. Conditioned serum free medium (CSFM) from nineteen-day fetal rat lung cultures was shown to contain several bioactive peptides as detected by 3H-Thymidine incorporation into chick embryo and rat lung fibroblasts, as well as 14C-choline incorporation into surfactant in mixed cell cultures. Using ion-exchange chromatography and Sephadex gel filtration, a partially purified mitogen, 11-111, was obtained. Although II-III cross-reacts in the somatomedin-C (Sm-C) radioimmunoassay, disc polyacrylamide gel electrophoresis demonstrates that this component has an electrophoretic mobility [Rf value] of 0.59 (+/-0.02) and does not co-migrate with Sm-C in this system (Rf = 0.53 ) and, thus, is probably not authentic Sm-C. The partially purified II-III stimulates mitosis in chick embryo fibroblasts and post-natal rat lung fibroblasts. Multiplication in fetal rat lung fibroblast cultures is stimulated only when these are pre-incubated with a competence factor or unprocessed CSFM. This suggests the existence of an endogenously produced competence factor important in the regulation of fetal lung growth. Preparation II-III does not possess surfactant stimulating activity as assessed by 3H-choline incorporation into lipids in predominantly type-II cell cultures. However, a peak of surfactant stimulating activity was found to elute off Sephadex G-75 at a Kav = 0.23 (MW approx. 13 Kd) and was distinct from the mitogenic II-III peak (Kav = 0.50). These data demonstrate the presence of a maturational/ mitogenic factor, influencing type-II mixed cell cultures. In addition, II-III had been shown to play an autocrine role stimulating the proliferation of fetal lung fibroblasts. Finally, these data suggest the existance of a local produced competence factor.
Typescript.; Thesis (Ph. D.)--University of Hawaii at Manoa, 1985.; Bibliography: leaves 103-111.; Photocopy.; Microfilm.; x, 111 leaves, bound ill. 29 cm
Tue, 01 Jan 1985 00:00:00 GMThttp://hdl.handle.net/10125/94181985-01-01T00:00:00ZMontes, Ana MariaEndotoxin protection of rats from oxygen toxicity : role of lung phagocyteshttp://hdl.handle.net/10125/9417
Endotoxin (1 mg/kg body weight, i.p.) greatly reduces lung damage and pleural edema in rats exposed to > 99% oxygen. Endotoxin also activates and depletes complement in vitro. Both complement and polymorphonuclear leukocytes (PMN) have been shown to play a role in the development of lung damage in several models of lung inflammation. PMN may injure tissue by releasing free radicals or proteolytic enzymes. This dissertation was designed to evaluate the possibility that the mechanism of endotoxin protection involves changes in either 1) the number of PMN or their ability to release free radicals or 2) serum complement levels following exposure of rats to > 99% oxygen for up to 3 days at 1 ata (sea level). The potential of 1avaged phagocytes to generate free radicals was determined using zymosan stimulated chemiluminescence (CL). Values were then expressed as peak CL/106 PMN. PMN peak CL fell progressively with time of oxygen exposure. Peak CL by PMN from saline pretreated rats breathing oxygen for 3 days was 80% lower than peak CL by PMN from paired rats pretreated with endotoxin. In addition, complement hemolytic activity was not altered in serum from endotoxin pretreated rats following exposure to > 99% oxygen or air for 65 hours. Depletion of complement in rat s prior to oxygen exposure also failed to provide protection from the pleural edema of oxygen toxicity. These results suggest that endotoxin does alter the ability of alveolar PMN from oxygen breathing rats to release free radicals but does not alter serum complement. a
Typescript.; Thesis (Ph. D.)--University of Hawaii at Manoa, 1985.; Bibliography: leaves 82-92.; Microfilm.; vii, 92 leaves, bound ill. 29 cm
Tue, 01 Jan 1985 00:00:00 GMThttp://hdl.handle.net/10125/94171985-01-01T00:00:00ZBerg, John TownsendEffects of chronic subpressor norepinephrine infusion on afterload-induced cardiac hypertrophy in ratshttp://hdl.handle.net/10125/9416
Thesis (Ph. D.)--University of Hawaii at Manoa, 1982.; Bibliography: leaves 260-277.; Microfiche.; xiv, 277 leaves, bound ill. 29 cm
Fri, 01 Jan 1982 00:00:00 GMThttp://hdl.handle.net/10125/94161982-01-01T00:00:00ZSiri, Francis MichaelResponse and regulation of vasopressin and renal function during graded exercisehttp://hdl.handle.net/10125/9415
Three series of experiments were conducted to study the response and regulation of plasma vasopressin during exercise. The renal handling of water and solutes during exercise was also investigated. Six male subjects, performed a graded exercise test on a treadmill to voluntary maximal effort. Three additional experiments were performed; a control and 1 hr of exercise at 35 and 70% of maximum heart rate. Blood samples were obtained at 20 and 60 min of exercise and after 1 hr of recovery. Urine samples were also obtained. Plasma vasopressin (PAVP) was unchanged during controls and 35% exercise and elevated following 60 min of 70% exercise, from 0.8 ± 0.2 at rest to 2.1 ± 0.3 µU/ml. This elevation persisted through recovery. Maximal exercise produced an increase in PAVP from 0.9 ± 0.1 to 2.7 ± 0.7 µU/ml after 20 min. Plasma vasopressin returned to resting levels following 1 hr of recovery. Plasma osmolality, blood pressure, plasma renin activity (PRA), and oral temperature were elevated during exercise. Plasma volume and body weight decreased. Plasma cortisol exhibited no change. A reduction of vasopressin metabolism may have occurred, contributing to the elevation of PAVP. There was no consistent relationship of changes in these parameters to the elevation of PAVP during exercise. Urine flow was decreased for both 70% and maximal exercise post-exercise and after 1 hr of recovery. The decrease immediately after exercise was accompanied by a decrease in creatinine clearance and osmotic clearance (Cosm) and an increase in CH2O. Recovery Cosm was decreased, CH2O increased, and creatinine clearance normal. The response of vasopressin to an elevation in body temperature was studied in seven males. The subjects underwent a 2-hr equilibration period, a l-hr experimental exposure, and 2 hr of recovery. The experimental exposures were a control, exercise, and passive elevation of body temperature, in a manner similar to that observed during exercise. Five-hour urine samples were obtained. No difference was noted in rectal temperature during exercise and passive temperature elevation. Urine flow was significantly reduced during exercise compared to control values. Vasopressin excretion was increased 22,79, and 17% for control, exercise, and passive temperature elevation, respectively. The increase in the excretion of vasopressin with exercise occurred in six of the seven subjects with no change seen during passive body temperature elevation. Seven subjects performed maximal exercise following dehydration (10 hr of fasting) and hydration (ingestion of 300 ml of water). The pre-exercise plasma osmolaiity of 283 ± 2 mOsm/kg for hydration was lower than that of dehydration (288 ± 2 mOsm/kg). Following exercise no difference was observed in osmolality. Plasma vasopressin after exercise was elevated, 0.6 ± with hydration and 1.8 ± 0.6 µU/ml with dehydration. No differences in PRA, plasma cortisol, mean arterial pressure, oral temperature, change in plasma volume, or workload and duration were noted between the two treatments. Urine flow was greater during hydration pre-exercise and post-exercise compared to dehydration. Post-exercise urine flow was reduced with dehydration, and for both treatments flow was reduced during recovery. Osmotic clearance was reduced post-exercise and through recovery, while CH2O was increased post-exercise with dehydration. Plasma vasopressin was elevated during exercise and appeared to be dependent on the hydration state of the individual, work intensity, and duration. Although the regulation of vasopressin during exercise was unclear, the elevation of vasopressin appeared to be independent of the dehydration which occurred during exercise. The elevation of PAVP apparently was not responsible for the occurrence of the antidiuresis associated with exercise, which was probably due to a reduction in glomerular filtration rate and sodium reabsorption.
Typescript.; Thesis (Ph. D.)--University of Hawaii at Manoa, 1979.; Bibliography: leaves 86-97.; Microfiche.; xii, 97 leaves ill. 29 cm
Mon, 01 Jan 1979 00:00:00 GMThttp://hdl.handle.net/10125/94151979-01-01T00:00:00ZWade, Charles EThe thermal physiology of tunahttp://hdl.handle.net/10125/9414
Photocopy of typescript.; Thesis (Ph. D.)--University of Hawaii at Manoa, 1979.; Bibliography: leaves 200-215.; Microfiche.; xv, 215 leaves ill. 28 cm
Mon, 01 Jan 1979 00:00:00 GMThttp://hdl.handle.net/10125/94141979-01-01T00:00:00ZBrill, Richard WalterBioinformatic approach for tracking HIV-1 evolution in Vietnam and neighboring southeast Asian countrieshttp://hdl.handle.net/10125/7035
There is high prevalence of a methionine substitution at the tip of the V3 loop (MGPGQ) among HIV CRF_AE strains from Vietnam. The aim of this study was to identify other molecular markers or ""signature sequences"" for mapping the spread of HIV in Vietnam and in neighboring Southeast Asian countries. Analysis of the sequence diversity and grouping by molecular markers suggested that ET strain initially gained entry in CSW in southern Vietnam. Unique substitutions among ECM and EC- strains in southern Vietnam IDU and CSW suggested independent introduction and spread of HIV among these high-risk groups. Unique and identical amino acid substitutions found in ECV strains from IDU in northern Vietnam and southern China suggested cross-border travel of virus-infected IDU.
viii, 69 leaves
Mon, 01 Dec 2003 00:00:00 GMThttp://hdl.handle.net/10125/70352003-12-01T00:00:00ZIsami, FumiyukiControl of the Coqui frog, Eleutherodactylus coquihttp://hdl.handle.net/10125/7034
Eleutherodactylus coqui is an invasive species whose unchecked population growth is having environmental and social impacts on the Hawaiian islands. One focus was to fine tune doses of possible toxicants to control the frogs. It was found that applied as a spray, a 1% caffeine and 0.01% pyrethrin cocktail yielded complete mortality in a single application. These concentrations could be tested in field trials. Animals treated with the caffeine/pyrethrin cocktail experienced decreases in liver and muscle glycogen and severe hyperglycemia. This is consistent with known phosphodiesterase inhibition triggering enzyme inhibitions that ultimately lead to lethality. IBMX, a caffeine analogue and potent phosphodiesterase inhibitor, when combined with pyrethrin, had a similar effect. Drugs blocking other possible modes of action such as adenosine antagonism and ryanodine receptor opening had no effect. It was therefore suggested that caffeine in combination with pyrethrin might be an effective method for controlling frog populations and the lethality of the treatment may be due to phosphodiesterase inhibition followed by eventual hyperkalemia.
vii, 32 leaves
Mon, 01 Dec 2003 00:00:00 GMThttp://hdl.handle.net/10125/70342003-12-01T00:00:00ZHutchinson, Robert BMarkers of cardiac injury in ultraendurance runnershttp://hdl.handle.net/10125/6969
Ultraendurance sports, allowing athletes eager to test the limits of their endurance, are becoming increasingly popular in the United States and throughout the world. The numbers of 100 mile running events; Ironman-distance triathlons (2.4 mile swim, 112 mile bike ride, 26.2 mile run); and multi day, multi-sports events such as the Eco Challenge are increasing. To date, few researchers have investigated the effects these ultraendurance events have on the human heart. In the early 1990's William Rowe suggested that permanent cardiac injury could develop in some endurance athletes in the absence of coronary atherosclerosis. Injury to the coronary endothelium as a result of endurance exercise could occur in athletes participating in multiple events if sufficient time is not allowed for endothelial repair. Rowe proposed that high levels of circulating catecholamines produced by endurance exercise might cause acute myocardial ischemia, patchy fibrosis, as well as coronary vasospasm (sudden, transient constriction of blood vessels). The vasospasm then produced high-sheer endothelial turbulence thus injuring the endothelium. These injuries suffered overtime would adversely affect the heart (Rowe 1992; 1993). In a review of catecholamine cardiotoxicity, Rona stated that the release of catecholamines during exercise might deplete the energy reserves of cardiac muscle cells and this depletion could ultimately result in necrosis. Moreover high-circulating levels of catecholamines might increase cardiac-muscle cell-membrane permeability (Rona 1985) Do events that test the upper limits of human endurance in fact have any adverse effects on the heart? If so, what are they? Are these effects transient or permanent? What is the minimum level of effort at which injury is first observed? These questions prompted this study and the results will contribute to the limited but increasing knowledge regarding the cardiac effects and/or side effects of ultraendurance exercise.
vii, 65 leaves
Thu, 01 May 2003 00:00:00 GMThttp://hdl.handle.net/10125/69692003-05-01T00:00:00ZCaroll, Patricia AThe Effect of Heavy Metals on the Uptake of L-Histidine by the Polychaete Nereis Succineahttp://hdl.handle.net/10125/6957
Integumentary uptake of 3H-L-Histidine by Nereis succinea was measured in the presence and absence of selected heavy metals and inhibitors in 60% artificial seawater (ASW). At low concentrations of L-Histidine (10 uM), metals stimulated L-Histidine uptake from ASW. Higher concentrations of metal inhibited L-Histidine uptake. In amino acid kinetic experiments, 0.5 uM Zn2+ significantly (P < 0.003) increased both L-Histidine influx Jmax (control: 4.7 ± 0.4; treatment: 15.3 ± 1.7 nmol/g dry weight x 15 min), and Km (control: 23.8 ± 5.1; treatment: 44.0 ± 8.8 uM). Fe3+ (0.5 uM) stimulated influx of 10 uM L-Histidine (Jmax = 6.9 ± 0.4 nmol/g dry wt x 15 min; Km = 86.7 ± 12.3 uM), but neither Ag+ nor Al3+ significantly (P > 0.05) altered amino acid influx. L-Leucine (25 uM) reduced Zn2+ -stimulated L-Histidine influx, suggesting a possible role of the Na-independent L-transport system in metal-stimulated L-Histidine transport by worm integument.
vii, 35 leaves
Sun, 01 Dec 2002 00:00:00 GMThttp://hdl.handle.net/10125/69572002-12-01T00:00:00ZPeppler, Jessica EliseThe Effect of Zinc on the Transmural Transport of L-H-Histidine in the Intestinal Epithelium of the American Lobster, Homarus Americanushttp://hdl.handle.net/10125/6947
It has been demonstrated that in rat erythrocytes, L-histidine enhances the transport of zinc (Aiken et al., 1992). These experiments also indicated that histidine uptake in rat erythrocyte is partially sodium dependent and shows inhibition by leucine. These observations suggest the involvement of the L-system carrier which is capable of transporting histidine with the participation of sodium ions. Similar effects have been shown to occur in the rat intestine (Wapnir et al., 1983). Other work has been conducted testing zinc absorption in rats and the effects of amino acids (histidine, cysteine, tryptophan and proline) on this process (Wapnir & Stiel, 1986). This study determined that histidine assisted in the transport of zinc in the jejunem and ileum of the rat. Further evidence shows that metals stimulate amino acid transport in crustacean hepatopancreatic cells. Monteilh-Zoller, Zonno, Storelli, and Ahearn (1999) showed that zinc doubled the transmembrane transfer of L-proline in lobster hepatopancreatic brush border membrane vesicles. The enhanced uptake of the amino acid in the presence of the metal was found to be due to increased 3H-L-proline maximal transport velocity (i.e. Jmax), rather than due to a change in binding affinity (i.e. Kt) induced by the metal. The L-proline transport occurred by way of a specific transport protein, the IMINO system. These studies indicate that zinc and histidine form a complex that is transported together. It is thus postulated that zinc enhances the transport of histidine. In this study, the effect of zinc on the transmural flux of L-histidine across the intestine of the Atlantic lobster (Homarus americanus) was investigated. Previous studies of amino acid transport involved alanine, a non-essential amino acid, which was largely metabolized by the tissue (Wyban, Ahearn & Maginniss, 1980). However, in this study, L-histidine, an essential amino acid for the growth of lobsters and other crustaceans, was the nutrient considered (Factor, 1995). Experiments support the hypothesis that the uptake of L-histidine is increased in the presence of zinc (Ahearn, H.R.H. et al, 2000; Liou & Ellory, 1990). The first portion of this project determined the net transmural flux of 3H-L-histidine at five different concentrations, in the presence and absence of a defined zinc concentration. Unidirectional transepithelial transport was measured across the intestine as a function of time. These measurements established that transport is likely carrier-mediated, as a saturation of a carrier molecule will limit transport. The second portion of the described research studied the influence of varying the concentration of zinc at a constant concentration of 100 µM L-histidine. The concentrations of zinc ranged from 5 µM to 250 µM. The optimal concentrations of zinc, which produced maximal carrier-mediated activation, were determined to be between 25 µM and 50 µM.
vi, 44 leaves
Sun, 01 Dec 2002 00:00:00 GMThttp://hdl.handle.net/10125/69472002-12-01T00:00:00ZForry, Erin PatriciaEcology and biology of the rough-toothed dolphin (Steno bredanensis)http://hdl.handle.net/10125/1194
Greater knowledge of the rough-toothed dolphin, Steno bredanensis, is needed to effectively contribute to conservation and management efforts for this species. The primary purpose of this research was to describe ecological and biological parameters for S. bredanensis that will be useful in future assessments of population stress. Several approaches were used to study S. bredanensis, including investigations of free-ranging populations, dead specimens, and captive individuals. Free-ranging rough-toothed dolphins distributed near small oceanic island environments were found to be more commonly sighted in-shore than off-shore. In the Windward islands of French Polynesia, this species preferred water depths of 1000 to 2000m and a distance of 1.8 to 5.5 km from the barrier reef. Group sizes ofrough-toothed dolphins sighted in French Polynesia range between 1 and 35 individuals with a mean size of 12.1. Endocrinology data for S. bredanensis was established in captive healthy and stranded individuals. Ranges and means were provided for progesterone, testosterone, cortisol and thyroid hormones. Changes in thyroid hormone concentrations were reflective of health status and testosterone appeared to be suppressed in ill individuals. Reproduction in S. bredanensis was investigated by determining the size and age range that this species attains sexual and physical maturity. Female rough-toothed dolphins attain sexual maturity by 9 to 10 years of age and males between 5 and 10 years at a similar length of approximately 216 cm. Physical maturity is generally reached at an older age and larger size for both males and females. Ecologically healthy and unheahhy populations of S. bredanensis were described in this investigation and these fmding will be useful in assessing future threats to this species.
Sun, 01 Dec 2002 00:00:00 GMThttp://hdl.handle.net/10125/11942002-12-01T00:00:00ZWest, Kristi LeeAltered chemoreceptor response and improved cycling performance following respiratory muscle traininghttp://hdl.handle.net/10125/991
Cross-sectional studies have shown that well trained endurance athletes frequently have a lower peripheral and central chemoreceptor response (pRc and cRc) and a lower minute ventilation (Ve) during exercise compared to untrained individuals. Some recent prospective studies support these observations. We speculated that the reductions in chemoreceptor response and Ve may be the specific result of the high rates of ventilation occurring during endurance training. To test this idea, subjects performed voluntary eucapnic hyperpnea to simulate exercise hyperpnea while avoiding the metabolic consequences of physical exercise. We therefore examined the effects of respiratory muscle training (RMT: 20x30min sessions of voluntary eucapnic hyperpnea) on the pRc, cR, cycling performance, and Ve. Twenty endurance trained cyclists were randomized into RMT or control-groups. To indicate cRc both the hypercapnic ventilatory response at rest (HCVRr) and during light exercise (HCVRex) were measured in a background of 50% O2. The pRc was assessed by measuring the ventilatory response to a modified Dejours O2 test (4-6 trials of 10-12 breaths of 100% O2) during light exercise. Endurance performance and Ve were measured during a fixed-rate cycling endurance test, performed at 85% of the maximal workload until exhaustion. The RMT-group's cycling endurance improved significantly compared to controls (+3.26±4.98min versus -1.46±3.67min. p=0.027) but Ve was unchanged at all times analyzed. The pRc was significantly reduced in the RMT-group but unchanged in controls (-5.8±6.0% versus +O.1±4.6%, p=O.032). The cRc, both at rest and during exercise, was not significantly altered following RMT in either group. However, the X-intercept of HCVRex exhibited a significant shift to the left (-5.83±10.68mmHg, +O.38±2.48mmHg, p=O.047, RMT-group and controls respectively). The importance of this leftward shift and the reduced pRc, though statistically significant, is unclear because there were no significant changes in Ve during any test nor were there correlations between Ve or performance or the altered chemoreceptor responses. We conclude that exercise hyperpnea, as simulated by RMT in this study, is accompanied by a reduction in pRc and a leftward shift in the HCVRex, and improves cycling endurance; however, the altered chemoreceptor responses had little impact on Ve suggesting that their role in the control of ventilation during exercise is minor.
Thu, 01 May 2003 00:00:00 GMThttp://hdl.handle.net/10125/9912003-05-01T00:00:00ZMcMahon, Michael E.The effect of dietary salt on bone in a genetically-defined rat underloading/overloading modelhttp://hdl.handle.net/10125/989
One the most serious health hazards of aging and of long term space flight is the loss of bone. The most important determinant of the debilitation due to bone loss is the peak bone mass achieved during late adolescence, which itself may be influenced by gender and environmental factors such as mineral balance. Sodium intake is considered a risk factor for both hypertension and osteoporosis. It is estimated that 30-60% of the population is hypertensive and 30-40% of the population is salt sensitive. The primary purpose of the present studies was to both delineate and combine the effects between salt
intake and salt sensitive hypertensive genotype on bone. Our hypothesis was that hypertensive rats would have more severely affected bone than normotensive rats due to
salt supplementation and/or genotype. In addition, how these effects might be altered by
immobilization/overloading stress was examined as this further burdens NASA space
pioneers. This study investigated the possible effects of an ad libidum 1% or 2% saline
instead of water on the normotensive (W) and salt sensitive hypertensive (SS) young
female rats. A total of 46 weight-matched female rats (7 weeks old) were used. Treated
rats in the 1% study drank 1% saline ad libitum for a 42 day salt supplementation period,
beginning at day 7 (after arrival) to day 49. Treated rats in the 2% study drank 2% saline
ad libitum for a 42 day salt supplementation period, beginning at day 7 (after arrival) to
day 49. The right hindlimb of each animal was immobilized by binding to the abdomen
with 4 layers of elastic bandage tape, the hip joint in flexion and the knee and ankle joint in extension for the 42 day salt experimental period. Body weight and urine volume was
measured biweekly. Food and fluid intake was monitored daily. After sacrifice, three
sites (both the underloaded and the overloaded tibiae, as well as the L-2 vertebrae) were
processed for histomorphometric analysis. The wet weight (g) and length (mm) of the
excised right immobilized and left overloaded femur and the ulna were measured. A 3-point bending test was applied to femurs only. Immediately after the femur breaking strength measurements, bone was cut transversely, one mm from breaking point (fracture
location), and a 1.0 mm cross-section was cut for morphological measurement. In
addition, a 5 mm high cylinder section from each femur was cut and used for bone
composition measurements along with the right ulna bone. A number of elements were
analyzed at one time with Induced Coupled Plasma (ICP) spectrometry. The systolic
blood pressure and heart rate were measured in the 6th week of study by the tail-cuff
sphygmomanometer method. A more robust result was seen with increased concentration of saline treatment from a 1% saline threshold level, to the 2% saline level. Using two-way ANOVA, both hypertensive genotype and 2% saline treatment significantly increased blood pressure and heart rate, and decreased femur magnesium. The SS rat had significant reductions in bone mass, femur cross-sectional area and zinc concentrations with simultaneous elevations in femur stiffness, strength and calcium concentrations. Two percent saline treatment markedly increased both blood pressure and heart rate and decreased both femurs magnesium and cancellous bone in the weight-bearing tibia bone. After 6 weeks of immobilization (to simulate space weightlessness), reductions in cancellous tibia bone volume, with elevations in femur bone stiffness, mineral concentration (calcium and phosphorus) and in trace elements (zinc and manganese) were found in the underloaded femur. Our findings suggest genotype, and saline treatment, and immobilization adversely affect bone in adolescent female rats. In addition, the deleterious bone effects are site specific, affecting each site differently.
Sun, 01 Dec 2002 00:00:00 GMThttp://hdl.handle.net/10125/9892002-12-01T00:00:00ZMoore, Kathleen Annikki